The Brain on Drugs

Notes: Article presented during the first Neuro-Aesthetics conference organized at Goldsmiths University, London UK, May 2005.
Drugs, Altered States of Consciousness and Cultural Production Section.

I’m going to try to give you a very brief neurological perspective on drugs, and how they interact with the brain, and what they might do to the brain. But as you heard, from Warren’s introduction, I am by no means, an expert on drugs (in both ways). I’ll try to give you an idea of what the current thinking is on how drugs impose themselves on the brain. To do so, I’m just going to give you a brief introduction to some of the main players of the brain. I’m going to talk a little bit about neural synapses, because the synapse are key in understanding what drugs do. Synapses are actually the location where drugs act in the nervous system. But synapses is also going to be very interesting for the whole conference because if you’re interested in plasticity and how the brain changes. By strengthening and weakening synapses, by taking them out and putting new ones in, changing the reliability of the synapses, we’re actually changing the neural network, how it is structured, how the architecture of it is, and how it functions. So, from a neurological standpoint, the synapses are going to be what the conference is about. It’s definitely central for drugs and what drugs do in the brain.

I would like to move on and show you that the principle way that drugs interact with the synapses and neural transmitters in the synapse is quite similar, no matter what drug is used. I’m going to give you an example to illustrate some of the biological mechanisms that are happening when drugs are introduced to the brain. During my ten minute talk, I would like address what changes are actually happening while drugs are in the system, and also whether there are long-term changes. Is it just something that happens while one is on the drug or are there any long-term effects that the drugs have?

Ok, so lets just plunge right into it. We have already heard that the brain contains millions of billions of neurons, and there are billions of connections between these neurons. These connections are made by synapses. Consciousness and cognition are based on the connectivity of this neural network. And this network is constantly changing. When we learn and when we have an experience, the connectivity is actually changing in a constant flux; there is nothing stable about your brain. You know; when you walked in this morning your brain was different than it is now; just because it is affected when we are sitting here talking. Synapses are basically the place where these changes happen. Synapses connect neurons and relay information that is more scattered in one neuron and it’s transformed through processes in the neuron to the next one. So synapses are basically the way the neurons interact with each other. The electric ones, the chemical ones that we are interested in, in relation to drugs and drug use, are chemical synapses. The chemical synapses used to convey information from one neuron to another are called neural transmitters. The neural transmitters you’re going to hear about, concerning drugs, are chemicals like dopamine and serotonin; I’m sure you have heard about them before. I’m going to show you a little diagram of synapses so you know what I am talking about when I am talking about a synapse.

So, in essence, you have two neurons. One that is incoming and a second one that has information it is going to deliver to the next neuron, which is down here {indicating on a diagram}. This information has to actually travel. So these neurons, these synapses, these post-synaptic neurons don’t really touch. There has to be a way of conveying the information from one neuron to another. In the cell, information is conveyed by electrical signals; and these electrical signals trigger the release of these molecules. In this case it is a dopaminic synapse. So dopamine is the transmitter. A spike or an electrical code of the nerve basically releases the chemical, the transmitter, which is then taken up by receptors on the other side in the second neuron and is then again transformed back into the electrical code in which the information is coded. So you see, there is no direct contact. You have to go via some chemical that crosses this gap, this bridge. I’m going to get back to the diagram of the synapse to explain to you one of the mechanisms of how drugs interfere with this process. The transmitters are in the gaps, the spaces between these neurons. And you have to imagine that there are a lot of cells around it. So it’s not an open space. It’s a nice, small, contained area. The transmitters are going to be taken up by the receptors, and then change the properties of the next neuron and convey information to the next neuron. Then the transmitters have to be moved up. It’s like you have a pinball in a pinball machine. It’s wiggling around there and every time it hit’s something, like a bell, something changes in the next neuron. Then the ball has to be sucked up again and taken out of the play. That happens by these molecules that are able to suck this neural transmitter up again and transport it back into the neurons where they were released from, so they are packaged again into these synaptic vesicles. Once information arrives, there is a release of this transmitter. [It] then finds the receptors and is then vacuumed away; moved up by these transporting molecules.

So what happens when drugs are used? One of the things that, for me, is quite interesting, is neural transmitters are the original side affect of the drugs. It’s like we are our own alcohol. This is, in a sense, quite true. The drugs act upon the synapses by interfering between the neural transmitter and the receptor. There are multiple ways this happens. Basically all drugs act upon the synapses. The effects, principle of their function in the brain, are very similar. The drug mimics the neural transmitter. It is very similar in it’s structure. So if you would have a drug in here it would look very similar to the dopamine, and instead of the dopamine, it would be able to connect to the receptors and start this information transfer. But now it would not be information that comes from the neuron before, but the drug acting on the receptors. Or, the drug can block the receptor. Basically, you have a drug that is similar in its structure to the dopamine. It would be able to actually connect to the receptor, but it just sits there. It doesn’t let go of the receptor. It blocks the dopamine from reaching the receptor. This way, it would influence and change the second carrying neuron, no matter whether this neuron would try to convey information to the second one. So it could try to release as many transmitters as it wanted and there would be no way for this transmitter to interfere with the receptor because the receptor is just blocked; there’s something sitting in there.

Another very common way that drugs interfere with the synapses and the transmitter system is that the drug inhibits the re-uptake of the drug; it inhibits this vacuum cleaner. And, as in this example with cocaine, cocaine doesn’t look at all like the neural transmitter. In this case of this depiction, you see it’s a turquoise diamond, whereas dopamine are these red triangles. So chemically it has nothing in common with the transmitter and it also couldn’t bind to the receptors. What it can do is bind to the transporter molecules. And because of that, the neural transmitter that is in that space can’t be taken up again. So in essence, the transmitter just stays there, and stays there, and stays there. It’s going to be bound to the receptor that it’s going to be released from. And because it can’t be re-taken up, it’s going to bind again, and again, and again. So, it’s like you have a barrage of information coming in through that neuron, whereas you actually just had one bit of information coming on, but because the cocaine sits there, it appears to the second neuron as if that first neuron was constantly active. So these are three ways that you can interfere and interrupt the information transfer between pre-synaptic and post-synaptic neuron and in this way change the way information is conveyed and change the way the network is actually constructed.

What I put down here, what I don’t know, or at least I couldn’t find, and I don’t think there is a lot of research on this, is how these changes in the information transfer are actually translated into the effects that drugs have; the reason why there are so many different effects of drugs on our mind and also on bodily functions: sweating, heart beat, the heart beat goes up, you get euphoric, hallucinations. We don’t really understand yet which part of the brain is responsible for that, and what happens in detail. The reason for this is that despite the fact that the principal actions of drugs on the brain are very similar it depends a lot on what transmitter system the drug is actually pinching on. Different transmitter systems have broadly different effects on the brain and on our physique. It also depends on what areas these transmitter systems are actually visiting of the brain. The areas of the brain they are visiting are very broad; it’s not a small, localized area of the brain.

This is a list of different drugs and what the effects are. Opiates are antagonists, which means they mimic our receptor; they mimic our transmitter for a receptor. In the case of opiates, it’s actually quite interesting, because they mimic endorphins, which are released when you eat chocolate or run really hard. It’s a pleasure. Our own brain makes a pleasure drug for us, endorphins. Opiates bind to the endorphin receptors and then, in turn, increase the amount of dopamine, which is in the brain. So your brain is washed in dopamine because of the opiates. LSD seems to be binding to serotonin receptor’s sides, yet we don’t really know how that creates hallucinations. Antagonists are drugs where the drug binds to the receptor. It doesn’t give the correct transmitter trans bind. So they are in competition with each other.

Cocaine, as I explained in a little more detail, blocks the re-uptake of dopamine. The same is true for ecstasy, amphetamines, and methamphetamines. They all block the re-uptake of different neural transmitters. You can see here how complex the whole drug issue is, because it’s not just on of these broad transmitter systems. In most cases it’s multiple systems that are actually affected. So cocaine not only blocks the re-uptake of dopamine, but also neurophon, and also of serotonin. The same is true for amphetamines and ecstasy.

Ecstasy causes a massive release of serotonin. It releases the stores of serotonin in the brain and it takes months to recreate those stores. So your brain is devoid of serotonin after ecstasy and it blocks its re-uptake.

Cannabis binds to the receptor for an endoorphin, which is a chemical found in chocolate; which I thought was kind of nice {laughing}. So if you don’t want to smoke, eat your chocolates and you might get the same effect. All these effects that I have noted here are really the short-term effects: What is happening when you are taking the drug. But there are effects that also have a longer time scale. A medium time scale lasts for hours or for days. For example, by changing the amount of neural transmitters that are there, or changing the time that receptors are occupied, the brain actually regulates the number of receptor sites and regulates the amounts of transmitters that it makes. So what happens on a short-term basis is you get a down regulation of receptor sites. You get a down regulation of the amount of transmitters that you make, which creates an imbalance of the drug. This is one of the reasons that, people believe, lead to drug addiction. The most interesting, for me, is the long-term effects that drugs can have. Long-term effects don’t mean you have to use drugs over and over and over again. Some of these effects are present after one or two or three exposures to drugs. All of these long-term effects have an affect on the connectivity of the network. One of the most interesting effects is that you can get long-term potentiation and long-term depression of subjectivity.

What this means is long-term potentiation and long-term depression are thought to be the mechanisms of the brain for learning. It means that it makes a synapse stronger or less strong, or more reliable or less reliable. This means that you are basically reinforcing circuits. So if you have long-term potentiation that would mean that a certain connection in the brain, a certain chain or a certain network, is going to be reinforced and reinforced and reinforced. You cannot only get this by learning or experience, but you can get these effects by the use of drugs. Different drugs create different long-term potentiation and or long-term depression in different parts of the brain. You can get changes in the synaptic connectivity and the architecture and function of the neuronal network. You can have changes in the neural activity and single cells as well as in populations of neurons. What changes in neural activity is whether a cell or a neuron is actually conveying the same amount of information before or after it was exposed to a drug. There are changes in gene conscription, which can lead to changes in the makeup of the neurons. In extreme cases, such as with ecstasy, it can lead to the death of synapses, the death of neural endings. With ecstasy, you’re really pruning neurons; you’re depleting the brain of some of its information transfer sites. All these biological changes affect the neural network. They affect plasticity. This plasticity, what drugs induce, is changing perceptions and is changing interpretations of the world. That goes back to some of the things talked about earlier, when people have eye opening new ideas and can relate to an object in a very different way than before. That might be due to things that have happened to their neural network, to their brains, because of the influence of the drugs.

Martina Wicklein studied biology at the University of Beyreuth and did her masters there in 1989 characterizing olfactory sensilla in termites. For her PhD (1990-1994) at the University Tübingen, she continued to work on sensory processing, but moved from smell to vision and from the periphery into the brain. The focus of her thesis was how visual interneurons code for motion in a very fast flying day-active moth, and she used her physiology (recording from single nerve cells in the awake moth) and anatomy as her techniques. She moved to the USA to the University of Tucson to continue her studies focusing on the neuronal implementation of depth perception, and continued that project including computational neuroscience and modeling approaches in addition to the physiology and anatomy that she had used before at the Salk Institute of Biological Studies in San Diego. Since 2004, she has been at University College London, working on color processing in bumble bees, combining behavioral studies and physiology, in order to elucidate the neuronal principles behind such phenomena as color constancy, brightness detection, and color vision in general.

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